Document XOynZDoYeBabvYben8472gv3J

GeorgiaF&cific intracompany memo to K. L. Gipson Irom T. E. Withycombe subiect Occupational Cancer location location dale PLAINTIFF'S EXHIBIT Portland Portland September 1, 1976 Ken, enclosed is article by the director of the Mt. Sinai School of Medicine,Environmental Health Sciences Center, which is one of the articles cited in a recent petition to the Consumer Product Safety Com mission to ban joint compounds containing asbestos. I believe you will find the article interesting and particularly the reference to sinus tumors on Page 3, footnote 17. You may wish to review the article cited. fc Enclosure cc w/enc. : Mr. F. G. Breuer ' C /,T. E. W. Gp 09 SGP 0008835 Kecenc rerspecuveb m Occupational Cancer BY IRVING J SELIKOFF In recent years, many previously unsuspected carcinogenic agents have been identified and new perspectives established for the evaluation of the increasing numbers of chemical substances introduced into the environment. Attention is sometimes called to the fact that the first neo plasms for which etiological factors could be established, were occupational cancers. The report 200 years ago by Percivall Pott of cancer of the scrotum in individuals who had been employed as chimney-sweeps (I), or that of chemical car cinogenesis in humans first described 80 years ago as "aniline cancer" (2), or that radiation-induced cancer had an occu pational starting point among miners in Schnccburg and Joachimstal almost 90 years ago (3), are cited. These claims arc true, yet it is equally true that each was an isolated de scriptive observation, of muffled impact in its time. Accelerated development of a connecting mature body of knowledge, the discipline of occupational cancer, has_ rathc_r. been a matter of tiic past two decades Although it was related to what went before by the continuing productive studies of the effects of carcinogenic aromatic amines (2), if one event can be said to be the origin of Ibis new phase, it may be the brilliant description in 1935 hv Richard Doll of the association between occupalional exposure to asbestos and an important risk of~dcnth of lung cancer (4). Doll's dcmoTistration of the applicability of chronic disease epidemiology provided an important example for future research. Many of the concepts we now take for granted in the evaluation of occupational carcinogenicity, as, the need for long periods of observation (5), the utility of cohort studies (6), the possibility of co existence of cancer and other biological toxicity (7), were in herent in bis classic report. Similar approaches base guided the best of experimental studies and have increased their relesancc *' I . ,u\ With this background, a good deal has been learned about occupational cancer in recent years. This has included identi fication of carcinogenic agents previously unsuspected of such effects and the establishment of a number of perspectives which are now available for the evaluation of other materials used in industry and/or agriculture or which may be intro duced in the future (9). The latter achievement is perhaps more important, since the number and complexity of new or re cently introduced agents has attracted much attention, and little is known concerning their carcinogenic potential LATENT PERIOD The above term is perhaps inexact since we do not actually know what is happening in tissues between the time of first exposure and initial evidence of clinical disease. Changes may be under way, albeit not detectable with current techniques Perhaps "period of clinical latency" or "lapsed period" would be more exact (10). In any case, each of these terms describes an important phenomenon --that a considerable time must usually elapse between onset of exposure to an occupational carcinogen and the first evidence of resulting cancer. General ly, this period is 20--35 years, although as little as 10--IS years may suffice, or 35--50 or more years will pass The time sequence can be affected by a number of variables touched on below, but it is remarkable how their influences operate with in relatively narrow constraints. Understanding this, two conclusions become evident I irsl, it would have been difficult or impossible to establish the carcinogenicity of substances widely introduced only in the SGP 0008836 k ! L t kll, , J .'.lit ( r . . I J............................ - .......................................... ........ w ttii K'ii/ciic .nul r.ulMlK'ii 1 o ftiul Me client i'f mi*.'!; '-til'- stances. .ifT'11'prTIiic' Minl/fs .1 re ncvcss.irv In see if *.\ic c\y>vs'Vsvi b.vekvivovnvd tales .ire increascsl Sometimes, espe- ci.illy if less common tumors are being considered. its brain or adrenal or kidney or lymphoma. extensive observations arc necessary, if not of moderate si/ed groups over lone periods of time (after tlic 20 scar point!), llten of scry large groups for shorter peiiods (to achieve an adequate number of "person- sears" of observation). In a number of instances, unusual tumors base been ob served in considerable numbers for ssbieb the usual espeeted- obsersed ratios arc almost superfluous. When cancer of the scrotum occurred among Pott's chimney sssceps the absence of biostatisticnl calculations did not present recognition of the unusual situation. Sinus tumors among^wopdworkers may be looked^ in somewhat the same light (17JL. Two "neoplasms. infrequent in general but common with industrial exposure, have demonstrated that such "signal"' tumors can be important factors in identifying occupational carcinogenesis. One. hemangiosarcoma of the liser. has as sumed such a role recently and sxill be discussed below. The second, mesothelioma, has a longer history. First reported in the pleural cavity of an asbestos worker in 1953 (IS) and in the peritoneum of another the next year (19). its link to asbestos was firmly established in J[960 (20) when, in a serics_q 47. eases in one laboratory in "'S6uih~ATrica7 over a five year period. 45 were shown to have had opportunity for asbestos exposure of one .or another type, decades before. The impact of this finding can be gauged by appreciation that, in general, approximately one in a thousand deaths in the general popu lation had been known to be caused hy these previously un common tumors. With occupational asbestos exposure, these tumors have proven common (21) In some cohorts of asbestos workers, approximately five or six percent of deaths have been due to pleural and peritoneal mesothelioma (5). In others, the percentage is lower; it has been reported, for example, that this neoplasm is less frequent among Quebec chrysotile asbestos miners (22). When found in family contacts, it led to the understanding of the danger of bringing dust from the factory to the home (23), when found amid residents in the neighborhoods about asbestos plants, it bespoke un controlled asbestos air pollution in the past. In South Africa's large series of eases, with adequate history, only approximately fifteen percent have been judged not to have had some known asbestos contact (24). Thus. where vor mesqlheJi<ia\a_ii.found,, asbestos is sought. In this way. otherwise unsuspected oc cupational exposures to asbestos have been identified--in ship yards, especially (25). ENVIRONMENTAL CANCERS FROM OCCUPATIONAL SOURCES An important dimension was added to occupational cancer with the discovery that neoplasms might occur with the dis semination of the agent beyond the factory gate, either by its release during the manufacturing process or from resulting waste, or by contamination of households with the offending material being brought heme on workers' clothes. Although instances of such disease had been known before (20), the full import of the problem was not appreciated until Newhouse's report in 1965 (23) when she demonstrated that, of 76 con firmed cases oT mesothelioma in the files of the London Hos pital, of the..4? not. known to have had occupational exposure tojisbcstos, nine had simply lived in the households.oLasbestos workers ("conjugal disease") and 11 had neither worked with the material nor lived with someone who had been so em ployed, but had resided, many years before, within one half mile of an asbestos plant in London. This finding was soon confiitiled (26), and the principle of carcinogenic risk derived from occupational sources is an important factor in current evaluation of control of environmental cancer, whether it he from radiation-producing power sources, agricultural use of pesticides, air and water pollution from petrochemical industry operations, carcinogenic mineral dust, or other substances or processes (II) These considerations arc separate from those involving cancer risk with end-product use, either during further industrial manipulation of materials or in utilization of consumer products. SGP 0008837 Ibcie was a onions discrepancy dining the fust li.df of (|,is century between continued concern re-guiding the potential for occupational cancer in the burgeoning petrochemical industry and reliable evidence that this was occurring with any fre quency. In considerable part, the contradiction remains. On the one hand, the industry deals with a very large number of chemicals which either have been shown to have carcinogenic potential in laboratory animals, or are related to these chemi cals, belonging to such suspect groups as the polycyclic aroma tic hydrocarbons or some of the halogcnatcd hydrocarbons: in several instances, as benzpyrene or /J-iiaphthylaminc. occupa tional cancers in humans have been clearly established. On the other hand, the number of chemical agents so incriminated has remained comparatively small and the number of workers involved, limited. With the recent identification of vinyl chloride induced cancer (27. 28). the situation has changed somewhat. It is still not known whether a good many of the petrochemical industry's materials will turn out to be carcinogenic--in large part, an adequate "Intent period" has yet to run its couisc. to allow for proper evaluation. Still, to find that a key chemi cal in the giant plastic industry was clearly carcinogenic has been disconcerting. Further, it was sobering to realize that if vinyl chloride's carcinogenicity had been expressed in increased risk of cancer of lung or colon, elevated rates of neoplasms of these sites among the affected workers might not have been identified for some years, at the earliest. Tbe_fact.t|iat it was an unusual tumor, hemangiosarcoma of the liver, otherwise rare in the general population (perhaps one in 10 000--40 000 deaths), which occurred, attracted attention. Three cases in one plant, the B F Goodrich Company in Louisville, Kentucky, were sufficent to establish a strong sus picion of the risk (29) and the suspicion became a virtual certainty when the same neoplasm was found in other vinylchloride polymerization plants, making vinyl chloride the likely offender, rather than other coexisting chemicals, as special additives or process chemicals, peculiar to the Louisville plant's operation. At the same time, the fact that only a dozen and a half cases came to notice in the first five months after discovery of the condition did little to allay concern, since these cases, when analyzed, had begun work, on the average, approximately 20 years before death, at a lime when the vinyl chloride-polyvinyl chloride industry was limited in size and still employed relatively few workers. Of the 19 cases recorded by mid-June, 1974, 15 had begun work 1944--1952, with an overall average of 20.4 years from onset for the group as n whole. Since the great majority of workers in vinyl chlo ride-polyvinyl chloride plants were first employed during the 1950s and 1960s, it was evident that the full impact of vinyl chloride tumors would not be known for another two decades. Limited data so far available suggests that, at least for poly vinylchloride polymerization workers, the incidence of oc cupational cancer will he significant. We have examined the mortality experience of a cohort of workers employed at a large polyvinylchloride polymerization facility in the United States. The plant opened in 1946 and from that year to 1963, 257 individuals were employed in the production process for five years or more. While exposures began in 1946, relatively few individuals were employed prior to 1951, when a significant increase in the work force took place. Thus, the majority of (he cohort has had a hare 20 years or less from onset of exposure. An initial report of the experience of these men has been made (30). We have traced each of the 257 individuals to December 31, 1973. Twenty-five were found to have died, of all causes. Three of tbe__deaths, each confirmed at autopsy, were due to hemangiosarcoma of the liver (Table 4). Ages at death were 41, 54. 60. Elapsed time from onset of first expo sure to death was 14, 17, 23 years. DOSE-DISEASE RESPONSE RELATIONSHIPS Discussion of this thorny question, with social, ethical and economic implications co-minglcd with scientific perspectives, was stimulated and made much more acute in the evaluation of regulatory measures necessary for the control of vinyl chloride cancer. While it has been generally agreed that the risk of malignancy increases with intensity and duration of exposure, there has been much less concordance in the evalu- m.isI 3*1 M> )c,us. until llic I.M ilvv.ulc m mi NuimkI. wv Mill potential than those unliv iduallv cupaMc ol iiuiuom' ui.,lw. ool 'k iii'lo,'with pioscii ViuaiJcilgc, to identify c.iiKcr risk iu nancy, and since at least some vvotking environments now tend hvtiMtn of recently introduced .incuts for unoihor (no oc cvcn__ (o become more complex, this may turn out lo be of consider \\ytct vVet .vvWs (11). amt cpiilcmiolugy must look to assistance able practical importance in the future. front other ilisciplincs. 1`arcnlhctically, a similarly long period Second, animal studies generally arc diiccted to the investi must elapse before it can lie ascertained whether measures gation of one agent; negative results may therefore Ivc mis designed to correct an occupational cancer hazard arc actually leading insofar as actual work risk is concerned. (To com effective. This has been .the ease, for example, among nickel pensate, one should hasten to add. dosages can be far greater smelter workers (12). than those which occur in industry, and carcinogenicity en I nc importance of the principle of clinical latency has per hanced). haps nowhere Itccn better demonstrated than with lung cancer associated with occupational exposure to asbestos. In cur SIGNAL CANCERS Laboratory, we have been following a cohort of asbestos in Most occupational cancers arc identified as occurring as in sulation workers, composed of all 17 800 members of the creased numbers of common malignancies. Thus, increased Union of such workers in the United States and Canada on rales (taking age, year and sex into account) of lung cancer January I, 1967 (5). By December .11. 1972, 1356 of these men occur, for example, with occupational exposure lojaje, chro had died, almost -100 more than had been expected. There mates, arsenic, nickel carbonyl, uranium mining, fluorspar were ^5._dcaths_of.lung cancer, whereas only 56 had been mining, hematite, /3-chlormcthylcther and asbestos; of bind- anticipated. Analysis of the work history of these men indi cated that the_exccss deaths ^wcrc...|argcJL>_JunitCd_to_lhosc_ jworkers who had achieved more..than.20 jears XCflm. onsct _of_ tlic.i r_w ork (Tables. 1. and. 2). The risk of lung cancer with occupational exposure to asbestos could easily be missed, and inaccurate conclusions drawn, if studies are made without the opportunity to ob Table 1. Expected and observed deaths among 17 800 asbestos Insula* serve a sufficient number of indiv iduals 20--30 or more years lion workers In the United States and Canada January 1, 1967--Decem from onset of work exposure. Similar results have been ob ber 31, 1972. tained in studies of uranium miners (13) and workers in nickel refineries (14) and with other agents; indeed, when many lung Duration from onset of exposure cancers arc seen after significantly shorter periods, as with Less than 20 years More than 20 years /)-chlormcth)lether (15), one might justifiably suspect rather Expected* Observed Expected* Observed intense exposure or particularly virulent agents. Total deaths--alt causes 203 90 249 756.12 1109 MULTIPLE FACTOR ETIOLOGY Investigations of occupational exposures for carcinogenicity Cancer all sites Lung cancor Asbestosis AM other causes 30.42 8.40 __* 173.40 64 145.13 28 47.47 7 178 610.99 511 247 94 504 generally seek to isolate the suspect materials. This is reason Number of persons 12 681 5119 able. Nevertheless, this approach is in a sense artificial, since carcinogenic agents arc infrequently used singly, but rather in complex work environments, often with a variety of other substances of unstudied potential, and by individuals whose personal and social environments are equally varied. The Expected rates are based upon age-specific white mate death rate data of me US National Office of Vital Statistics. Rates (or 1972 were extra polated from rates trom 1967--1971. US rates are not available, but these are rare causes of death in the general population. possibility of interaction of two or more agents has long been known in the experimental setting; since 1968 it has been shown for occupational cancer in humans as well (16). Jt was found among asbestos workers, for example, that lung cancer risk was not significant!) increased among those men who did Table 2. Deaths from lung cancer among 17 600 asbestos insulation workers in the CD and Canada, January 1, 1967--December 31, 1972; relation to elapsed period from onset of work exposure. not also have a history of cigaretie smoking. Those_who did, "had much more lung cancer than cigarefle'srnokers.in general^ Lung cancer "Asbestos exposure thus markedly increased the lung cancer risk of cigarette smoking; it has been calculated that an Years from onset Expected deaths* Observed deaths Ratio asbestos worker who smokes cigarettes has 92 times the risk of death of lung cancer compared with an individual of the same age who neither smokes nor works with asbestos (16). The powerful multiplying effect of the combination of two agents can be appreciated by examining the experience of asbestos insulation workers cited above. When the cohort was established, the smoking habits of the majority of the workers was recorded; 9590 had a history of cigarette smoking, 609 had a history of pipe and/or cigar smoking but no cigarette smok <10 10--14 15--19 20--24 25--29 30--34 35--39 40--44 45--49 50 + Total 0 66 1.97 5 87 9 55 10.70 8 20 4 68 4 84 4 51 4 97 55 87 0 s 25 23 3 9 34 36 56 60 , 52 73 29 6 2 27 5 6 19 4 2 22 4 4 275 4 9 ing, and 1457 had never smoked at all. Their mortality experience, with particular reference to lung cancer, is detailed in Table 3. _Amone those who never smoked, only, one lung cancer w.as seen from January I. 1967 through DeccTivTk? ITTT9T2, The pipe .and _C'gat 5n\oking_group.;vlso.Jtad_ Expected deaths are based upon age-specihc white male death rate data of the US National Office of Vital Statistics Rates for 1972 were extra* polated from data from 1867--1971. SGP 0008838 only one. lung fqnccr death. On the other hand, there were "179 lung cancer deaths among those with a history of cigarette smoking, although only 32 such deaths were expected to occur.' This, despite the fact that all of these men had worked in the Table 3. Expected and observed deaths of lung cancer among 17 800 US and Canada asbestos Insulation workers, January 1, 1967--Decern* ber 31, 1972; relation of cigarette smoking. same trade, with equal opportunity for occupational exposure to asbestos. The significance of the principle of multiple factor inter No of persons Deaths (tom lung cancer Expected* Observed Ratio action has many ramifications. Two arc of immediate interest. First, some substances, by themselves, may, have no carcinogemc effect; in concert with oTlicrs. m-.ilign.w]vyjiuiy_i>ciJUL_ "finch influence may be additive or multiplicative (theoretically, Smoking habits not known History of cigarette smoking No history or cigarette smoking Nover smoked History of p>pe and or cig.if only 0144 9590 2066 1457 603 16 76 31 60 7 51 4 40 3n 94 5 6 179 5 7 2 03 1 02 1 03 there could also be a protective effect, as well). As a corollary, substances now deemed innocuous may change their habit in new circumstances; our vigilance must be constant Too. since Expected doaths basod upon agospocitic US mortality rates for while mates disregarding smoking Lung cancer estimates based upon US ralos v cancor Of tung, pleura, bronchus nnd Ir.ichoa. categories 16? and 16) of tho international Classification of Discasos end Causo* of Ooaths, Tab'o 4. C/tusc* of death omung 25 workers oxposed to vinyl chloildo for S or ryears. Cancers o1 all sites______________ t^roanQiosarcoma of Itvor 3 Nr jplosms ol lymphntic and hcmatopoiotic hssuoi2 Dram (Glioblastoma) Puncroas Colon Dona Cirrhosis (with csophapcal vancas) Post-opcrillvt bleeding (Cholotithiasit Cardiovascular disease*, other______________________ 9 1 1 1 1 1 14 ation of whether a lower threshold existed below which cancer would not occur. There have been few data bearing directly on this aspect of the question and, in the nature of things, it might be that such data arc unlikely to appear. "Negative" experi ments, to be convincing, would have to involve very large numbers of animals and, more important, observation of very large numbers of vinyl chloride workers exposed for pro longed periods of time at measured low levels of exposure to the monomer. Even if these data should be obtained, they would always be only an approximation, since further study conceivably could show exceptions. Theoretical considerations would seem to indicate that there is no identifiable lower, threshold limit for carcinogenic agents (31). The proposed regulations for the control of occupational exposure to vinyl chloride in the United States seem to approach the problem from this point of view; a level of one part per million has been proposed (32) which, interpreted in practical terms, might be considered a "no threshold" level but one which allows for inevitable mistakes and accidents which might occur in the industrial environment, as well as recognition of practical problems concerned with instrumental monitoring of the work environment. PRETESTING OF NEW MATERIALS Recognition of the long period of clinical latency between onset of exposure to materials in the occupational environment and their carcinogenic effect, if this is to occur, has recently raised the corollary question xvhether_we^ighLanjicipaLe_sucl3, evaluation andj.bortervot eliminate,- this period.of-uncertaity. Much attention is now being paid to this possibility. Until 'recently, however, expectation and desire exceeded promise. Although structural similarity to known carcinogens might occasion a high level of suspicion, cancer potential does not necessarily follow structural resemblance; many exceptions are known. Further, while suspicion could be directed to agents with biological activity other than cancer, many are known with toxic effects on kidney, liver, lung, central nervous sys tem, without concomitant recognized cancer potential. Experiences with vinyl chloride and /j-chlormcthylcthcr suggests, however, that laboratory scrccning.mighL be.feasible, or at least some agents. In each instance, laboratory studies were able to establish the carcinogenicity of a chemical sub stance which was later shown to be carcinogenic in man (28, 33). It is not known whether such experimental screening ap proaches will he equally productive with other agents, nor whether other laboratory techniques, including mutagenic studies, will extend their utility (31) Certainly, this is to be hoped for and much work, is being initiated to provide infor mation on the question. Guidelines that would point priorities for selection of agents to be tested arc also being discussed, and include such considerations as chemical structure, evidence of other biological activity, number of workers likely to be exposed. For substances already in use, similar considerations could apply, with lltc added dimension that epidemiological studies should be suggested when there arc available groups of nUrncoi and Nolo: t. I* Pore. Canter of the Strotntn. Clururgual Ohscnattons () I.< u ci Ot.irL and Col ling*, Izvndnn, 1775) pp 63-6*. 2. J C Arens and M l: Argui Chemical inthtetiitn of Cancer (Academic Pren. New York. 1974) Vol lilt pp 3 - 4. 3. A Tirehan and It Sikl. American Journal of Cancer 14, 681 (1932). 4. R Doll, British Journal of Industrial Medicine 12, 81 (1953). 5. I J Selikoff. E C llantmond and II Seidttt.in. in Huilugieal effects of Asbestos, P Bogovski, J C Gilson. V Timbrell and J C Wagner, Eds (International Agency Rrearch on Cancer, Lyon, 1973) pp 209--JI6. 6. T F Mancuso and E J Coulter. Archives of Environmental Health 6 (2). 210(1963). 7. I J Sefikoff, J Churgand E C Hammond, Journalofthe American Medical Aisoetalion III, 22 (1964). I. J C Wagner, G Berry, J W Skidmore and V Timbrell. British Journal of Cancer It, 252 (1974). 9. E C Hammond and I J Selikoff, in Analytic and Experimental Epidrmiohgv of Cancer, W Nakahara, 1 Hirayama, K Nishioka and H Sugano. Eds (University of Tokyo Press, Japan. 1973) pp 41 - -49. TO. I J Sefikoff and E C Hammond, Environmental Research 4 (2) ii --iii (1971). 11. I J Selikoff and C Hammond, Proceedings of the 7th national Cancer Confer ence, Los Angeles. 687(1973). 12. R Doll, L G Morgan and F E Spcizcr, British Journal of Cancer XXIV (4) 623 (1970). 13. F E Lundin. Jr, J W Lloyd. E M Smith, V E Archer and D A Holaday, Health Physics 16, 571 (1969). 14 E Pedersen, A Hogelveit and A Andersen, International Journal of Cancer 12 32 (1973). 15. W G Figueroa, R Raskowski and W Weiss, Hew England Journal of Medicine 281(21). 1096(1973). 16. 1 J Selikoff. E C Hammond and J Churg. Journal of the American Medical As sociation 204(2). 106(1968). 17. E D Achciao.RJtCo*dclLaa<LE.RMit.Jtriiish JournalofIndustrial Medicine 21 .JUIWU 18. A W'eiss, Medtsinische 3. 83 (1954). 19. F Letcher, Archivfiir Cenerpaihologic und Cewerbehygienr 13. 382 (1954). 20. J C Wagner, C A Sleggs and P Marchand, British Journal of Industrial Medicine 17, 260(1960). 21. J B Enticknap and W J Smilher, ibid21. 20(1964). 22. J C McDonald, A McDonald. G W Gibbs. J Siemiatycki and C E Rossiter, Ar chives of Environmental Health 22.677(1971) 23. M L Newhouse and H Thompson. British Journal of Industrial Medicine 22, 261 (1965). 24. 2 Webster, South African Medical Journal 47 (5). 165 (1973). 25. P G Harries, Annals of Occupational Hygiene II. 135 (1968). 26. J Licben and H Pistauka. Archives of Environmental Health 14, 559 (1967). 27. PL Viola. A Bigotti and A Caputo. Cancer Rtseareh 31.516 (1971) 28. C Maltoni and G Lefemine, Environmental Research 7, 381 (1974). 29. J L Creech and M N Johnson, Journal of Occupoiionat Medicine 16, 150 (1974). 30. W J Nicholson, H Seidman, E C Hammond and 1 J Selikoff, Annais of Hew York Acadtmy ofSciences, in press. 31. Evaluation of environmental carcinogens. Report to the Surgeon General. USPHS, April 22,1970, Ad Hoc Comm nice on the Evaluation of Low Levels of En vironmental Chemical Carcinogens. 32. IIS Department of Labor Occupational Safety and Health Administration. Expo sure to vinyl chloride, occupational safely and health standards (Federal Register 39:35890-35898. October 4. 1974) 33. B L Van Duuren. B M Goldschmidt. C Katz. L Langseth. C Mercado and A Sivak. Archixes of Envirunmrntal Health 16. 472(1968). 34. U Rannug, A Johansson. C Ramel. C A Wachlmcistcr Ambto 3. 194 (1974) 35. Research supported by grant ES 00928 of the National Institute of Environmental Health Sciences and by the Environmental Cancer Research Project of the Ameri can Cancer Society R-53 B. Dr Selikoff serves as Professor ol Community_Mcdicln<; at Jhq Mount Sinai School of Medicine ol the City University of Net* York; and ,as Director--ol-its..Environmental Health Science Center. A past President of the New York Academy of Sciences, his Interests now emphasize problems of environmental cancer, particularly those associated with materials In Industry. How ever, his research has In the past also Included other diseases; and for many, his achievements In environmental disease re* search arc matched by his contributions In the introduction of Isonlazld for the chemotherapy of tuberculosis, tor which he was honored by tho Lasker Award of tho American Public Health Association in 1955. His address: Mount Sinai School of Modi* cine, Filth Avo and 100 Street, New York. N Y 10029, USA. r SGP 0008839